Background and study aims: Endoscopic submucosal dissection (ESD) has become widely accepted as a minimally invasive treatment for early gastric cancer (EGC), and opportunities to use ESD to treat EGC in elderly patients are increasing. The objective of this study was to elucidate the safety and efficacy of ESD in elderly patients. Patients and methods: Between April 2006 and March 2013, a total of 892 patients with EGC were prospectively recruited to undergo ESD according to definite inclusion criteria. The short-term outcomes and incidence of complications in 345 of these patients who were 75 years of age or older (elderly group) were compared with the short-term outcomes and incidence of complications in the remaining 547 patients (non-elderly group). Factors associated with the occurrence of pneumonia and delirium were also investigated. Results: The R0 resection rate did not differ between the two groups (96.2 % in the elderly group vs. 96.7 % in the non-elderly group; P = 0.65). The incidence of pneumonia (7.5 % vs. 1.8 %; P < 0.01) and incidence of delirium (10.1 % vs. 1.1 %; P < 0.01) were significantly higher in the elderly group. The incidence of post-ESD bleeding and incidence of perforation were similar in the two groups. No emergency surgery was required, but one patient in the non-elderly group died of aspiration pneumonia. On multivariate analysis, age 75 years or older, cerebrovascular disease, chronic obstructive pulmonary disease, delirium, and remnant stomach or gastric tube were independent risk factors for pneumonia, and age 75 years or older, diabetes, dementia, and pneumonia were independent risk factors for delirium. Conclusion: ESD for EGC was feasible for elderly patients in good condition. However, pneumonia and delirium may develop more frequently after ESD in elderly patients with co-morbidities.
In patients with liver cirrhosis, treatment with diuretics can increase zinc excretion by suppressing the reabsorption of zinc through renal tubules, which might lead to zinc deficiency.
The toxic effects and changes in biochemical markers related to kidney and bone in depleted uranium (DU)-injected rats were examined in order to clarify the relation between clinical biochemical markers and the degree of damage in these organs. Male Wistar rats received a single injection in the femoral muscles of 0.2, 1.0 or 2.0 mg kg(-1) of DU which was dissolved in nitric acid solution adjusted to pH 3.2, for comparison with the group injected with nitric acid solution, and the control group. Urine and faeces were collected periodically over a 24 h period. Thereafter, the rats were killed at 28 d after DU injection. The body weights of the DU-injected groups decreased dose-dependently for the first 3-7 d, and then began to increase. The DU concentrations in the urine and faeces decreased rapidly within 3-7 d after DU injection. Urinary N-acetyl-beta-D-glucosaminidase (NAG)/creatinine peaked at the third day after DU injection, with a high correlation to the injected DU doses. There were high correlations among the injected DU doses, DU concentrations in the kidney and urinary NAG/creatinine values that were obtained at 28 d, respectively. The blood urea nitrogen (BUN) and creatinine in the serum also showed a high correlation with the DU-injected doses. The results indicated that urinary NAG/creatinine, BUN and creatinine in serum were useful indicators to diagnose the renal damage by DU, as well as to estimate the DU intake and concentration in the kidney when the intake is >2 mg kg(-1) DU. The total bone mineral density of the proximal metaphysis of the tibia decreased in the 2 mg kg(-1) DU group. In addition, alterations of the trabecular bone structure by inhibiting bone formation and promoting bone resorption were observed by bone histomorphometery. The bone biochemical markers osteocalcin, tartrate-resistance acid phosphatase, pyridinoline and rat-parathyroid hormone increased in all the DU injected groups, indicating that these markers were useful as sensitive indicators for diagnosing bone damage, even if the DU dose injected is low.
Thrombocytopenic patients with chronic hepatitis C virus (HCV) infection are poor candidates for antiviral treatment with interferon (IFN), but no standard treatment for thrombocytopenia has yet been established. We evaluated the safety of splenectomy and its efficacy for the initiation and continuation of antiviral therapy. From March 2003 to April 2006, 10 patients (mean age 62.5 years) with HCV-related cirrhosis, low platelet count (<==106 000/mm(3)) and splenomegaly (spleen size >==10 cm) underwent splenectomy. Platelet counts significantly increased at 4-8 weeks after splenectomy [pre: 64 200 +/- 6900/mm(3)vs post 209 000 +/- 40 600/mm(3) (P = 0.004)]. No severe operative complications were observed. All patients subsequently received antiviral therapy. Of the eight patients who were infected with HCV genotype 1 and had a high viral load (>==100 KIU/mL), four received combination therapy with pegylated IFNalpha-2b plus ribavirin, and the other four received standard IFNalpha-2b plus ribavirin. One patient infected with HCV genotype 2 and another with HCV genotype 1 and a low viral load (<100 KIU/mL) were treated with pegylated IFNalpha-2a. Six patients achieved sustained virologic response (SVR). Among four patients who failed to achieve SVR, one was given retreatment with pegylated IFN plus ribavirin, and the other three received low-dose long-term IFN therapy. Although this study was small, the treatment results were similar to those for patients without thrombocytopenia and suggested that splenectomy would not reduce the antiviral efficacy of IFNalpha-based treatment.
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